Neuroendocrine Tumour Unit - ENETS Centre of Excellence, Royal Free Hospital, London, NW3 2QG, UK.
St Mark's Academic Institute, Northwick Park, Watford Road, Harrow, HA1 3UJ, Middlesex, UK.
Curr Oncol Rep. 2022 Oct;24(10):1281-1286. doi: 10.1007/s11912-022-01211-5. Epub 2022 May 13.
Mesenteric desmoplasia in small intestinal neuroendocrine neoplasms (SINENs) is associated with increased morbidity and mortality. In this paper, we discuss the development of desmoplasia in SINENs.
The fibrotic reactions associated with these tumours could be limited to the loco-regional environment of the tumour and/or at distant sites. Mesenteric fibrotic mass forms around a local lymph node. Formation of desmoplasia is mediated by interactions between the neoplastic cells and its microenvironment via number of profibrotic mediators and signalling pathways. Profibrotic molecules that are mainly involved in the desmoplastic reaction include serotonin, TGFβ (transforming growth factor β) and CTGF (connective tissue growth factor), although there is some evidence to suggest that there are a number of other molecules involved in this process. Desmoplasia is a result of autocrine and paracrine effects of multiple molecules and signalling pathways. However, more research is needed to understand these mechanisms and to develop targeted therapy to minimise desmoplasia.
小肠类癌肿瘤（SINENs）肠系膜纤维组织增生与发病率和死亡率增加相关。本文讨论 SINENs 中纤维组织增生的发展。
与这些肿瘤相关的纤维反应可能仅限于肿瘤的局部环境和/或远处部位。肠系膜纤维性肿块围绕局部淋巴结形成。纤维组织增生是通过肿瘤细胞与其微环境之间的多种促纤维化介质和信号通路相互作用介导的。主要参与纤维反应的促纤维化分子包括 5-羟色胺、TGFβ（转化生长因子 β）和 CTGF（结缔组织生长因子），尽管有一些证据表明有许多其他分子参与这一过程。纤维组织增生是多种分子和信号通路自分泌和旁分泌作用的结果。然而，需要进一步的研究来了解这些机制，并开发靶向治疗以最小化纤维组织增生。
